Alterations in Bidirectional Transmembrane Calcium Flux Occur Without Changes in Protein Kinase C Levels in Rat Aorta during Sepsis
Abstract
A depression in aortic contractility has been previously demonstrated in rat intraperitoneal sepsis and during endotoxemia. In this study, we determined whether the mobilization of extracellular calcium (using calcium 45) and the release of intracellular calcium are altered in septic rat aorta when compared to sham-operated controls. The concentration of protein kinase C was also determined by using 3H phorbol-12,13-dibutyrate (PDBu). We found that calcium influx was unaltered under basal conditions but that the ability of norepinephrine (NE) to augment influx was significantly depressed (P <. 05;CONTROL VS. SEPTIC, 572 + OR - 54?SE vs. 428 + or - 30 micro mol calcium 2+/ kg dry wt. aorta). Calcium influx stimulated by high K+ was unchanged in aortae between control and septic animals. In the presence of NE, calcium efflux (an indirect measurement of intracellular calcium release) was significantly diminished (P < .001) in aortae from septic rats. The concentration of aortic protein kinase C as assessed by PDBu binding sites was unaltered in septic rats when compared with controls. In conclusion, we found that during sepsis alpha-adrenergic receptor activation of both calcium influx and efflux by NE is decreased; these alterations could be related to the depressed aortic contractility observed in sepsis. Keywords: Neurochemicaltransmission, Calcium channels, Reprint.
Document Details
- Document Type
- Technical Report
- Publication Date
- Nov 01, 1988
- Accession Number
- ADA203246
Entities
People
- B. L. Roth
- J. A. Carcillo
- R. Z. Litten
Organizations
- Armed Forces Radiobiology Research Institute